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Cancer-associated snaR-A noncoding RNA interacts with core splicing machinery and disrupts processing of mRNA

Sihang Zhou1, Simon Lizarazo2, Sandip Chorghade3

  • 1Department of Cell and Developmental Biology, University of Illinois Urbana-Champaign, Urbana, IL, USA.

Nature Communications
|November 25, 2025
PubMed

Insights

Small RNA A (snaR-A) promotes cancer cell proliferation by disrupting mRNA splicing. Depleting snaR-A enhances splicing and reduces tumor growth, identifying it as a potential cancer driver.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • RNA Biology

Background:

  • Cancer cells exhibit increased RNA polymerase III activity, activating normally silent small RNA genes.
  • Small NF90-associated RNA isoform A (snaR-A), a hominid-specific noncoding RNA, is implicated in cancer cell proliferation via unknown mechanisms.

Purpose of the Study:

  • To elucidate the mechanisms by which snaR-A influences cell proliferation in cancer.
  • To investigate the interaction of snaR-A with cellular machinery involved in mRNA processing.

Main Methods:

  • Investigated snaR-A interactions with mRNA splicing factors, including SF3B2, a U2 small nuclear ribonucleoprotein (snRNP) subunit.
  • Assessed the impact of snaR-A overexpression and depletion on intron retention and mRNA splicing efficiency.
  • Correlated snaR-A levels with cell proliferation rates and splicing characteristics in primary cancers.

Main Results:

  • snaR-A interacts with splicing factors and localizes near splicing machinery in subnuclear foci.
  • Overexpression of snaR-A leads to increased intron retention, indicating inefficient splicing.
  • Depletion of snaR-A enhances splicing of specific mRNAs and reduces cancer cell proliferation.

Conclusions:

  • snaR-A acts as a molecular antagonist of mRNA splicing, contributing to cancer progression.
  • Dysregulation of splicing by snaR-A represents a novel, non-mutational mechanism driving tumorigenesis.
  • snaR-A-mediated splicing perturbation may mimic splicing defects caused by U2 snRNP mutations in cancer.

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